Cannabis Is Curing My Cancer and Now I Want It Legalised

Joy Smith was diagnosed in July 2016 with ovarian cancer. In August 2017 she was given six weeks to live after it was discovered that the cancer has spread to her stomach and bowel. But now she’s in remission and claims cannabis oil cured her terminal disease. Research Consultant Matthew Atha explains why the research into cannabis oil has been so limited.
Broadcast on 13/03/2018

 

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A friend of this blog has healed his prostate cancer!

Posted today by Ken, in response to Dennis Hill and his great work. Dennis is still in remission. (See this post  for more.)

 

I would like to thank you Dennis from the bottom of my heart for telling your story and providing me with the knowledge and method to treat my stage 2b prostate cancer. Over the past 4 years, I had 4 biopsies and 9 PSA tests which showed a slow increase in cancer growth. I did the full 9 month treatment using your protocol and then had an MRI. My prostate had returned completely back to normal! It was painless and easy to do without any psychoactive effects.
Words cannot express my gratitude to you. You’re work and videos are truly a gift to humanity! Bless you Dennis Hill. –Ken

The endocannabinoid system and cancer: therapeutic implication

From the British Journal of Pharmacology

An excerpt:
Screen Shot 2018-12-03 at 4.05.08 PM.png“Several mechanisms are likely to underline the pro‐apoptotic effects of cannabinoids and explain their anti‐cancer effects. Cannabinoids induce de novo synthesis of ceramides, a family of lipid molecules composed of sphingosine and a fatty acid, found in the cell membrane. Synthesis of ceramide occurs via activation of the enzyme ceramide synthase and leads to downstream activation of an extracellular regulated kinase (ERK) signalling cascade. This process results in cell cycle arrest and apoptosis. Activation of either CB1 or CB2 receptors triggers the ceramide‐ERK signalling pathway to promote apoptosis. (Figure 1 above). The increase in ceramide can also activate the p38 mitogen‐activated protein kinase (p38MAPK) pathway which can lead to apoptosis through multiple mechanisms (i.e. through activation of cysteine proteases (i.e. caspases) or through cytochrome C release from mitochondria). The sustained activation of ERK also promotes the induction of cyclin kinase inhibitor (p27/KIP1) which modulates regulatory molecules of the cell cycle (cyclins, cdks) resulting in cell cycle arrest and apoptosis…”

To read the full paper, click here

The dual neuroprotective–neurotoxic profile of cannabinoid drugs

From British Pharmacological Society

Abstract

Extensive in vitro and in vivo studies have shown that cannabinoid drugs have neuroprotective properties and suggested that the endocannabinoid system may be involved in endogenous neuroprotective mechanisms. On the other hand, neurotoxic effects of cannabinoids in vitro and in vivo were also described. Several possible explanations for these dual, opposite effects of cannabinoids on cellular fate were suggested, and it is conceivable that various factors may determine the final outcome of the cannabinoid effect in vivo. In the current review, we focus on one of the possible reasons for the dual neuroprotective/neurotoxic effects of cannabinoids in vivo, namely, the opposite effects of low versus high doses of cannabinoids. While many studies reported neuroprotective effects of the conventional doses of cannabinoids in various experimental models for acute brain injuries, we have shown that a single administration of an extremely low dose of Δ9‐tetrahydrocannabinol (THC) (3–4 orders of magnitude lower than the conventional doses) to mice induced long‐lasting mild cognitive deficits that affected various aspects of memory and learning. These findings led to the idea that this low dose of THC, which induces minor damage to the brain, may activate preconditioning and/or postconditioning mechanisms and thus will protect the brain from more severe insults. Indeed, our recent findings support this assumption and show that a pre‐ or a postconditioning treatment with extremely low doses of THC, several days before or after brain injury, provides effective long‐term cognitive neuroprotection. The future therapeutical potential of these findings is discussed.

Read the full text here

Growing hemp is about to be legal for the first time in nearly a century

CBD derived from Hemp will no longer be in a legal grey area

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Verge

[On November 29], Congress reached an agreement on proposed legislation that could make hemp legal to grow in the United States for the first time in nearly a century. Hemp may be derived from the same plant as marijuana, but it doesn’t make anyone high and is commonly used in food, fuel, and bracelets. The new legislation officially acknowledges the difference between the two.

Technically speaking, hemp is a variety of the cannabis plant that contains less than 0.3 percent tetrahydrocannabinol (THC), the psychoactive ingredient in marijuana. Though its derivatives have been used for everything from textiles to medicine, hemp is currently everywhere in the form of a trendy ingredient called cannabidiol (CBD). Manufacturers promise that CBD will alleviate pain and depression and other health issues (despite a lack of solid evidence for many claims), yet CBD has lived in a legal gray area for years because of the tricky legal history of hemp.

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